Evidence map›Paper›PMID 36779851›Full record

ArticleeLife2023

Bone marrow Adipoq-lineage progenitors are a major cellular source of M-CSF that dominates bone marrow macrophage development, osteoclastogenesis, and bone mass.

Kazuki Inoue, Yongli Qin, Yuhan Xia, Jie Han, Ruoxi Yuan, Jun Sun, Ren Xu, Jean X Jiang, Matthew B Greenblatt, Baohong Zhao

Open access · goldFull text read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
9.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Youthfulness of marrow AdipoqBone research · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Kazuki Inoue *Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, United States.ORCID 0000-0001-6305-9374
Yongli Qin *Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, United States.ORCID 0000-0001-6133-0511
Yuhan Xia *Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, United States.
Jie HanThe first Affiliated Hospital of Xiamen University-ICMRS Collaborating Center for Skeletal Stem Cells, State Key Laboratory of Cellular Stress Biology, Faculty of Medicine and Life Sciences, Fujian Provincial Key Laboratory of Organ and Tissue Regeneration, School of Medicine, Xiamen University, Xiamen, China.
Ruoxi YuanArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, United States.
Jun SunPathology and Laboratory Medicine, Weill Cornell Medical College, New York, United States.
Ren XuThe first Affiliated Hospital of Xiamen University-ICMRS Collaborating Center for Skeletal Stem Cells, State Key Laboratory of Cellular Stress Biology, Faculty of Medicine and Life Sciences, Fujian Provincial Key Laboratory of Organ and Tissue Regeneration, School of Medicine, Xiamen University, Xiamen, China.
Jean X JiangDepartment of Biochemistry & Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, United States.ORCID 0000-0002-2185-5716
Matthew B GreenblattPathology and Laboratory Medicine, Weill Cornell Medical College, New York, United States.
Baohong ZhaoArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, United States.ORCID 0000-0002-1286-0919
Hospital for Special Surgery · USFirst Affiliated Hospital of Xiamen University · CNCornell University · USThe University of Texas Health Science Center at San Antonio · US

Funding

Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-JR01AR071463 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Baohong Zhao · 2017 to 2026
$4.0M
Regulation of bone homeostasis and remodeling by long noncoding RNA Malat1R01AR078212 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Baohong Zhao · 2021 to 2026
$2.2M
Mechanisms of inflammatory bone remodelingR01AR068970 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ZHAO, BAOHONG · 2016 to 2021
$1.9M
"Establishing Pathways for Endothelial Support of Bone Formation with SLIT3"R01AR075585 · NIAMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI GREENBLATT, MATTHEW BLAKE · 2020 to 2024
$1.8M
CSF-1 Gene Expression in Osteoclast BiologyR01AG045040 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JIANG, JEAN X · 2013 to 2017
$1.5M
NIAMS NIH HHS R01 AR068970NIAMS NIH HHS R01 AR071463NIAMS NIH HHS R01 AR075585NIAMS NIH HHS R01 AR078212NIA NIH HHS R01 AG045040NIH HHS AG045040NIH HHS AR068970NIH HHS AR071463NIH HHS AR075585NIH HHS AR078212
6 · The paper itself

Abstract

M-CSF is a critical growth factor for myeloid lineage cells, including monocytes, macrophages, and osteoclasts. Tissue-resident macrophages in most organs rely on local M-CSF. However, it is unclear what specific cells in the bone marrow produce M-CSF to maintain myeloid homeostasis. Here, we found that Adipoq-lineage progenitors but not mature adipocytes in bone marrow or in peripheral adipose tissue, are a major cellular source of M-CSF, with these Adipoq-lineage progenitors producing M-CSF at levels much higher than those produced by osteoblast lineage cells. The Adipoq-lineage progenitors with high CSF1 expression also exist in human bone marrow. Deficiency of M-CSF in bone marrow Adipoq-lineage progenitors drastically reduces the generation of bone marrow macrophages and osteoclasts, leading to severe osteopetrosis in mice. Furthermore, the osteoporosis in ovariectomized mice can be significantly alleviated by the absence of M-CSF in bone marrow Adipoq-lineage progenitors. Our findings identify bone marrow Adipoq-lineage progenitors as a major cellular source of M-CSF in bone marrow and reveal their crucial contribution to bone marrow macrophage development, osteoclastogenesis, bone homeostasis, and pathological bone loss.

Indexed as

Macrophage Colony-Stimulating FactorOsteogenesisAdiponectinAnimalsBone MarrowBone Marrow CellsCell DifferentiationHumansMacrophagesMiceMice, Inbred C57BLOsteoclastsAdiponectinADIPOQ protein, humanMacrophage Colony-Stimulating FactorAdipoQ-expressing progenitorsAdiposebonebone homeostasisbone marrowbone marrow adipocyte progenitorsbone marrow adipoq+ cellsbone marrow macrophagesCsf1immunologyinflammationmacrophageM-CSFmedicinemouseosteoclastosteoporosispostmenopausal osteoporosisscRNAseq

Identifiers

PMID36779851
PMCPMC10005769
OpenAlexW4320485294

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read94
identifiers read4
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.